Front. Endocrinol.
Sec. Diabetes: Molecular Mechanisms
Volume 15 - 2024 | doi: 10.3389/fendo.2024.1483512
Provisionally accepted
The final, formatted version of the article will be published soon.
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Background: Type 2 diabetes mellitus (T2DM) and osteoporosis are prevalent, interconnected chronic diseases that significantly impact global health. Understanding their complex biological relationship is crucial for improving patient outcomes and treatment strategies. Method: This review examines recent research on the mechanisms linking T2DM with osteoporosis. It focuses on how abnormalities in bone metabolism, autophagy, ferroptosis, and vitamin D receptor (VDR) gene polymorphisms contribute to osteoporosis in T2DM patients. Results: Our analysis indicates that T2DM is associated with reduced bone formation and increased bone resorption, which are influenced by hormonal changes, inflammation, and disrupted cellular signaling pathways. Additionally, increased perirenal fat thickness worsens osteoporosis through local inflammation and altered adipokine levels. VDR gene polymorphisms provide new molecular insights into this connection.Addressing the identified mechanisms with targeted management strategies may improve bone health in individuals with T2DM. Future research should explore these associations in greater detail to develop more effective prevention and treatment strategies.
Keywords: type 2 diabetes mellitus, Osteoporosis, bone metabolism, Autophagy, ferroptosis, Perirenal fat thickness, Vitamin D receptor gene polymorphism
Received: 20 Aug 2024; Accepted: 05 Dec 2024.
Copyright: © 2024 . This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
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